Although many industrial chemicals produce a central-peripheral neuropathy, the biochemical and pathological evaluation of the neurotoxic syndrome has been studied only in recent years. Recently, both leptophos (0-4-bromo-2,5-dichlorophenyl 0-methyl phenylphosphonothioate), a delayed neurotoxic insecticide, and n-hexane, a known neurotoxic agent, have been implicated in the neurologic defects which developed in some workers in the factory that manufactured and packaged leptophos. The purpose of this study is to evaluate the effect of n-hexane and related hexacarbons, i.e. methyl n-butyl ketone, 2,5-hexanediol and 2,5-hexanedione in the production of delayed neurotoxicity by EPN (O-ethyl 0-4-nitrophenyl phenylphosphonothioate), an insecticide known to cause delayed neurotoxicity in hens. The ability of subchronic dermal application of EPN to induce delayed neurotoxicity in hens and threshold level have determined in the first year. The production of neurotoxicity following exposure by inhalation of these solvents is being investigated. The effect of inhalation of n-hexane and other hexacarbons on the development of neurotoxicity with dermal exposure to "no effect" levels of EPN will be determined. The effect of these treatments on brain and plasma cholinesterases as well as on the hepatic microsomal enzyme activities will be studied. The pharmacokinetics and metabolism of 14C-labeled EPN will be carried out with and without exposure to n-hexane.